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Chronic Stress Exacerbates Cerebral Amyloid Angiopathy through Promoting NET formation [II]

ABSTRACT: Chronic Stress Exacerbates Cerebral Amyloid Angiopathy through Promoting NET formation [II]

PROVIDER: PRJNA1051139 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27182616_1.fastq.gz	Fastqsanger.gz
	SRR27182616_2.fastq.gz	Fastqsanger.gz
	SRR27182617_1.fastq.gz	Fastqsanger.gz
	SRR27182617_2.fastq.gz	Fastqsanger.gz
	SRR27182618_1.fastq.gz	Fastqsanger.gz

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Chronic Stress Exacerbates Cerebral Amyloid Angiopathy through Promoting NET formation [II]

Project description:Cerebral amyloid angiopathy (CAA) is the leading cause of vascular dementia among the elderly. Neuropsychiatric symptoms are commonly manifested in CAA patients but are usually considered as consequences of CAA pathology. Here, we report that chronic stress promotes CAA progression, which enhances deposition of amyloid protein beta (Aβ) in brain blood vessels and exacerbates subsequent brain injury. Mechanistically, neutrophil is implicated in CAA development. Aβ that accumulated in brain vasculature induces neutrophil extracellular traps (NETs) by activating STAT6 signaling, which inhibits neutrophil apoptosis and switches the programmed cell death toward NETosis. During chronic stress, circulatory Norepinephrine (NE) strengthens STAT6 activation in neutrophil and promotes NET formation, thus exacerbates the NET-dependent angiopathy. We demonstrate that inhibiting neutrophil chemotaxis towards brain or suppressing NET formation both ameliorate CAA severity in the context of chronic stress. Therefore, we propose that stress-associated psychological disorders and NETs are promising therapeutic targets in CAA.

2024-12-15 | GSE249924 | GEO

Chronic Stress Exacerbates Cerebral Amyloid Angiopathy through Promoting NET formation [I]

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Chronic Stress Exacerbates Cerebral Amyloid Angiopathy through Promoting NET formation

Project description:Chronic Stress Exacerbates Cerebral Amyloid Angiopathy through Promoting NET formation

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Chronic Stress Exacerbates Cerebral Amyloid Angiopathy through Promoting NET formation [I]

Project description:Chronic Stress Exacerbates Cerebral Amyloid Angiopathy through Promoting NET formation [I]

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Chronic Stress Exacerbates Cerebral Amyloid Angiopathy through Promoting NET formation

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-12-15 | GSE249926 | GEO

A Human Model of Cerebral Amyloid Angiopathy Using Neural Crest-Derived Vascular Smooth Muscle Cells

Project description:There is a growing recognition of cerebrovascular contribution to neurodegenerative diseases. Cerebral amyloid angiopathy (CAA), characterised by amyloid-beta (AM-NM-2) deposits in the walls of intracerebral and leptomeningeal arteries, is evident in a majority of AlzheimerM-bM-^@M-^Ys disease patients and aged people. Here, we leverage on human pluripotent stem cells to generate vascular smooth muscle cells (SMCs) from neural crest progenitors, recapitulating brain vasculature-specific attributes in AM-NM-2 metabolism. We confirm that the lipoprotein receptor, LRP1, functions in our neural crest-derived SMCs to mediate AM-NM-2 uptake and intracellular proteasomal degradation. Hypoxia significantly compromises the ability of SMCs in AM-NM-2 clearance by suppressing LRP1 expression. This enables us to develop an assay of AM-NM-2 uptake using the neural crest-derived SMCs with hypoxia as a stress paradigm. We then tested several vascular protective compounds in a high throughput format, demonstrating the value of stem cell-based phenotypic screening for novel CAA therapeutics and drug repurposing. We adopted our previous SMC differentiation protocol (Cheung et al., 2012) to differentiate this intermediate neural crest population using platelet-derived growth factor BB (PDGF-BB, 10 ng/ml) and transforming growth factor-beta 1 (TGF-M-NM-21, 2ng/ml) for another 12 days. The resultant neural crest-derived SMCs (NCSMC) were then characterised in comparison to neuroectoderm-derived SMCs (NESMC) (Cheung et al., 2012) and positive control, human brain vascular SMCs (BVSMC).

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Chronic Stress Exacerbates Cerebral Amyloid Angiopathy Through Promoting Neutrophil Extracellular Traps Formation.

Project description:Cerebral amyloid angiopathy (CAA) is the leading cause of vascular dementia among the elderly. Neuropsychiatric symptoms are commonly manifested in cerebral amyloid angiopathy patients but are usually considered as consequences of cerebral amyloid angiopathy pathology. Here, it is reported that chronic stress promotes cerebral amyloid angiopathy progression, which enhances deposition of amyloid protein beta (Aβ) in brain blood vessels and exacerbates subsequent brain injury. Mechanistically, neutrophil is implicated in cerebral amyloid angiopathy development. Aβ that accumulates in brain vasculature induces neutrophil extracellular traps (NETs) by activating STAT6 signaling, which inhibits neutrophil apoptosis and switches the programmed cell death toward NETosis. During chronic stress, circulatory Norepinephrine (NE) strengthens STAT6 activation in neutrophil and promotes NET formation, thus exacerbates the NET-dependent angiopathy. It is demonstrated that inhibiting neutrophil chemotaxis towards brain or suppressing NET formation both ameliorate cerebral amyloid angiopathy severity in the context of chronic stress. Therefore, it is proposed that stress-associated psychological disorders and NETs are promising therapeutic targets in cerebral amyloid angiopathy.

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Differential Roles of Astrocytic CSF1 in Alzheimer's Disease and Cerebral Amyloid Angiopathy: Insights from Transcriptomic Analysis

Project description:Alzheimer's disease (AD) and cerebral amyloid angiopathy (CAA) are neurodegenerative disorders characterized by the pathological deposition of amyloid-beta (Aβ) in the brain. Although both conditions share common pathogenic pathways, they exhibit distinct cellular manifestations and disease progression. Our study focused on the differential expression and role of astrocytic colony-stimulating factor 1 (CSF1) in these diseases. Using transcriptomic analysis of 248 brain tissue samples from the hippocampal-entorhinal system of 50 individuals, we identified a significant increase in CSF1 expression in the CA4 subfield of AD patients compared to a marked decrease in CAA. Functional investigations revealed that astrocytes with elevated CSF1 levels displayed neurotoxicity associated with AD-like pathology, whereas reduced CSF1 expression in astrocytes was linked to vascular damage typical of CAA. These findings suggest that CSF1 plays divergent roles in AD and CAA, contributing to their distinct pathological profiles. Our study highlights the potential of targeting astrocytic CSF1 expression as a differential diagnostic marker and therapeutic approach in managing these overlapping yet distinct neurological conditions.

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